The morphologic type and severity of the glomerular lesions resulting from the deposition of circulating immune complexes is dependent on both quantitative and qualitative factors. The purpose of this research is test the hypothesis that the class of the immunoglobulin in the immune complexes is one of these factors. Experimental models of IgG and IgM mediate immune complex glomerulonephritis will be developed in the rabbit by exploiting the differential IgG or IgM antibody response to immunization with heart-denatured or ultraviolet-irradiated DNA coupled to a carrier protein. soluble fragments of DNA of various sizes will be injected daily to produce a chronic immune complex nephritis. The use of such an antigen would allow one to control for immune complex size and isolate the effect of immunoglobulin class by comparing renal injury due to greater than 19S IgM complexes to that due to greater than 19S and less than 19S IgG DNA-anti-DNA complexes. The rate of clearance from the circulation of the various size complexes will be determined by sucrose density gradient centrifugation. As a subsidiary study, the models will allow evaluation of the role of a "planted" antigen in immune complex mediated glomerulonephritis. The antigen, the carrier protein MBSA, will be "planted" as part of DNA-anti DNA immune complex and radiolabeled antibody will be passively adminintered; the specific binding of antibody to MBSA will be quantitated and correlated with glomerular injury.